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[Cancer Research 46, 3834-3837, August 1, 1986]
© 1986 American Association for Cancer Research

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Lymphocyte-activating and Growth-inhibitory Activities for Several Sources of Native and Recombinant Interleukin 11

Edwin V. Gaffney2 and Shiow-Chuan Tsai

Department of Molecular and Cell Biology, The Pennsylvania State University, University Park, Pennsylvania 16802

Several native and recombinant forms of human interleukin-1 (IL-1) and recombinant murine IL-1 were assayed for their ability to inhibit the growth of cell lines established from malignant and nonmalignant human sources. The amount of growth-inhibitory activity was compared to the units of half-maximal [3H]thymidine incorporation in mouse thymocyte cultures exposed to IL-1. Three malignant human mammary cell lines (MCF-7, T47D, and MDA-MB-415) were growth inhibited in the presence of both native and the {alpha} and ß forms of recombinant human IL-1. MDA-MB-415 was most sensitive. Although most sources of IL-1 showed good correlation between units of activity and percentage of growth inhibition, native IL-1 from Genzyme Corporation induced a cytotoxic effect. Murine IL-1 was less growth inhibitory than the human forms of the monokine. Human embryonic lung (HEL), adult fibroblast (CRL 1445), and transformed milk (HBL-100) lines were not growth inhibited when tested against any IL-1 source. A lung carcinoma (CALU-1) and a colon carcinoma (SW-48) were not inhibited by either the {alpha} or ß forms of human recombinant IL-1.

1 Supported by Grant CA 33637 from the National Cancer Institute, Department of Health and Human Services.

2 To whom requests for reprints should be addressed.

Received 1/21/86. Revised 4/ 8/86. Accepted 4/30/86.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1986 by the American Association for Cancer Research.